title: Effects of interleukin-1 on cardiac fibroblast function: relevance to post-myocardial infarction remodelling.
abstract: The cardiac fibroblast (CF) is a multifunctional and heterogeneous cell type that plays an essential role in regulating cardiac development, structure and function. Following myocardial infarction (MI), the myocardium undergoes complex structural remodelling in an attempt to repair the damaged tissue and overcome the loss of function induced by ischemia/reperfusion injury. Evidence is emerging that CF play critical roles in all stages of post-MI remodelling, including the initial inflammatory phase that is triggered in response to myocardial damage. CF are particularly responsive to the proinflammatory cytokine interleukin-1 (IL-1) whose levels are rapidly induced in the myocardium after MI. Studies from our laboratory in recent years have sought to evaluate the functional effects of IL-1 on human CF function and to determine the underlying molecular mechanisms. This review summarises these data and sets it in the context of post-MI cardiac remodelling, identifying the fibroblast as a potential therapeutic target for reducing adverse cardiac remodelling and its devastating consequences.
authors.affiliation: Division of Cardiovascular and Diabetes Research, University of Leeds, Leeds, UK; Multidisciplinary Cardiovascular Research Centre (MCRC), University of Leeds, Leeds, UK. Electronic address: n.a.turner@leeds.ac.uk.
authors.forename: Neil A
authors.initials: NA
authors.lastname: Turner
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D005109:Extracellular Matrix / Q000378:metabolism; D005347:Fibroblasts / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D009203:Myocardial Infarction / Q000473:pathology*; D053573:Receptors, Interleukin-1 Type I / Q000502:physiology; D015398:Signal Transduction; D020257:Ventricular Remodeling
chemical_list: D007375:Interleukin-1; D053573:Receptors, Interleukin-1 Type I
keywords: Cardiac fibroblast; Interleukin-1; Myocardial infarction; Signal transduction pathways; Therapies